Chronic Kidney Disease (CKD) is a significant public health concern, impacting
approximately 10% of the global population. Annually, millions face mortality or require
renal replacement therapy due to CKD progression. Kidney fibrosis, a result of chronic
parenchymal damage from various glomerular and tubulointerstitial insults, is a primary
determinant of outcomes. Accurately assessing the extent and severity of fibrosis is
vital for diagnosis and treatment. However, Glomerular Filtration Rate (GFR) may not
diminish despite the presence of renal fibrosis, often until extensive damage occurs,
owing to the kidney's compensatory abilities. Additionally, GFR reductions may not solely
indicate chronic damage or parenchymal fibrosis.
GFR estimates using serum markers offer only rough approximations of kidney fibrosis and
can be misleading. The gold standard for assessing kidney fibrosis is a kidney biopsy.
However, biopsies are invasive, with potential complications and sampling errors, as they
assess less than 1% of the kidney parenchyma. Given the heterogeneous and patchy nature
of fibrosis within kidneys, the efficacy of biopsies is further questioned. Serial
biopsies to track fibrosis progression are also impractical.
The need for noninvasive, accurate fibrosis assessment has led to research into various
imaging techniques, including ultrasound and Magnetic Resonance Imaging (MRI). Among
numerous MRI techniques explored for fibrosis assessment, Magnetic Resonance Elastography
(MRE) appears promising. MRE, combining MRI with acoustic wave assessment, quantitatively
determines tissue viscoelastic properties in response to external mechanical vibration.
Initially developed for liver fibrosis assessment, kidney studies have shown that
MRE-determined stiffness mildly negatively correlates with CKD stages and positively with
fibrosis in renal allografts and diabetic kidneys. While kidney stiffness increases with
fibrosis in renal allografts, it decreases with GFR in diabetic nephropathy. In CKD
progression, marked by increased fibrosis and decreased GFR, these opposing effects on
renal stiffness could limit MRE's applicability in CKD patients. We hypothesize that in
early-stage CKD, when GFR is normal or slightly elevated, MRE could effectively determine
renal fibrosis severity. To date, no study has specifically explored renal fibrosis and
stiffness correlation in early-stage CKD.
Therefore, this study aims to evaluate renal fibrosis using multifrequency 3D-MRE-derived
stiffness as a surrogate marker. This involves detecting renal fibrosis prior to CKD
changes, distinguishing renal fibrosis from CKD stages, and comparing renal stiffness
with clinicopathological correlates in CKD patients.